Background: The mainstay of treatment for alcohol withdrawal syndrome is a symptom-triggered approach using benzodiazepines. Phenobarbital, however, is an interesting agent in this scenario for several reasons. It is famous for it is long duration of action. IV Phenobarbital has an onset of action of over 15 – 20 minutes, a duration of action of 10 – 12 hours and a half-life of 53 – 118 hours in adults [5]. But phenobarbital has several other characteristics that make it attractive in the treatment of alcohol withdrawal. Importantly, it works on the GABA receptor differently than benzodiazepines. First, it increases the duration (not frequency) the chloride channel is open. Also, chronic alcohol abuse can alter the GABA receptor making it less sensitive to benzodiazepines not barbiturates. And finally, at very high doses, phenobarbital can open the chloride channel independent of the presence of GABA. The authors of this paper sought to compare a phenobarbital-adjunct versus benzodiazepine-only approach for the management of alcohol withdrawal syndrome in the ED. Read more →

Calcium Channel Blocker (CCB) toxicity usually present with bradycardia and hypotension, but with preserved mental status. This can help differential from Beta Blocker (BB) toxicity, where the patients often have altered mental status.

Hyperglycemia is the other hallmark of CCB toxicity, which can help you differentiate from BB. This hyperglycemia may be a harbinger of impending circulatory collapse, so be on guard in a pt with CCB overdose, normal vitals and hyperglycemia

Don’t be afraid to use and infuse hyperinsulinemia-euglycemia therapy for BB and CCB toxicity. Have a frank and open conversation with your team about how it works to get everyone on board before your start.

TCA overdoses present with a a number of signs and symptoms including anticholinergic symptoms, AMS, hypotension and seizures. Once you identify the TCA toxicity, you’re going to start with fluids and pressors and then move on the antidote which is sodium bicarbonate 1-2 mEq/kg as a bolus followed by a drip. You want to keep pushing sodium bicarb until you see the QRS narrow

Background: Stress related gastrointestinal mucosal damage is a commonly encountered problem in the critically ill patients admitted to the intensive care unit. The incidence ranges from 0.6-7% and is decreasing partly due to aggressive resuscitation strategies and focus on early enteral feeding1. Damage to the mucosal integrity occurs in conditions associated with increased inflammation and reduced mucosal perfusion 2. Despite its decreasing incidence, stress related GI bleed remains a major challenge for the intensivist with many studies showing increase in mortality and ICU length of stay in these patients3.

Stress ulcer prophylaxis is recommended for critically ill patients at risk for GI bleed; the major risk factors include need for prolonged mechanical ventilation, coagulopathy, hepatic and renal failure. There is high quality evidence supporting the use of H2 receptor antagonists (H2RA) and proton pump inhibitors (PPI) in these patients. Many international surveys show that PPIs are currently preferred for acid suppression4. Though many randomized controlled trials support the use of PPI over other acid suppressants, there is clearly no recommendation regarding benefits of one group over the other. Alhazzani et al5recently published a network meta-analysis of 57 trials enrolling over 7000 patients that showed moderate quality evidence that PPIs are more effective than H2 blockers, sucralfate or placebo in preventing clinically significant GI bleed though there is a possible increase in risk for pneumonia with similar mortality. Another meta-analysis by Alshamsi et al showed that PPIs were more effective than H2RAs in reducing the risk of clinically important GI bleeding and overt GI bleeding without a significant increase in risk for pneumonia, mortality and ICU length of stay6

Furthermore, there is growing concern that acid suppression predisposes patients to increased risk for nosocomial infections like pneumonia and Clostridium difficile as well as cardiovascular events. This was demonstrated in a few randomized clinical trials as well as a few observational studies7,8. The authors of the current study aimed to evaluate the benefits and adverse events associated with the use of pantoprazole for stress ulcer prophylaxis in patients at risk for gastrointestinal bleeding9Read more →

Background: Syncope, defined as a transient loss of consciousness with spontaneous and complete recovery to pre-event status, is a common emergency department (ED) presentation. Near-syncope is frequently seen as well. Unlike syncope, near-syncope has a more nebulous definition often thought of as the feeling of oncoming syncope without a complete loss of consciousness. Regardless of definition, many providers consider syncope and near-syncope as two ends of a spectrum of disease with near-syncope being not as dangerous and syncope being more dangerous. The literature on this, however, is inconsistent with a 2009 study stating that near-syncope was a “low-risk” factor (Sun 2009) and a 2015 study showing the opposite (Thiruganasambandamoorthy 2015). Additional high-quality data in this area is needed to further elucidate the risk of near-syncope presentations in the ED.Read more →

Introduction: Beyond the Data

The evolution from eminence-based to evidence-based care has come to define bedside emergency medicine, with rigorous skepticism and scholarly consideration accelerated by the power of global connectivity. Where anecdote and opinion once drove therapy, clinicians now approach clinical conundrums with deliberate reflection, expecting—and at times demanding–ever-higher proof of perfection prior to implementing or incorporating therapies, tests, or approaches into their own practice. Such cogitation ensures excellence and safety and avoids pitfalls of over-adoption or confounding. Unfortunately, so many of our daily decisions are made in a space devoid of definitive data, and require a synthesis of relevant literature with our accumulated knowledge and experience—a departure from evidence-based medicine into the pragmatic world of evidence-informed medicine. It is only at this precipice—where studies and statistics simply don’t exist—that we change, where we push forward the boundaries of care, and develop not only experience, but the very questions which will define the next advances in emergency medicine. It’s with this in mind that we present this REBEL post, an entry not so much a look back on manuscripts which dictate our practice, but a treatise to help us look forward. To not inform, but to inspire thought and inquiry. Read more →